Repercussões locais e sistêmicas da isquemia gástrica experimental

Abstract

Gastric ischaemia is provoked by the absence or decreasing of the blood flow to the stomach and may be followed by tissue necrosis, when perfusion is not immediately reestablished. As result of gastric necrosis, local and systemic inflammatory response always occurs. The inflammatory mediators induce to a cascade of events in the whole body,followed by multiple organ dysfunction. The purpose of this study was to evaluate local and systemic disturbances due to gastric ischaemia.This study was performed on 20 male rabbits, divided into 4 groups (n = 5):Group 1: Control - laparotomy and removal of organs for study.Group 2: ligation and section of the gastric vasculature. Reoperation after 3 hours and removal of organs for study.Group 3: ligation and section of the gastric vasculature. Reoperation after 6 hours and removal of organs for study.Group 4: ligation and section of the gastric vasculature. Reoperation after 12 hours and removal of organs for study.Of all animals, blood samples were taken immediately before surgery and after the established time of ischemia. Renal, liver and pancreas functions were assessed by mean of blood count and laboratorial exams. The whole liver, spleen, kidneys, stomach, pancreas, lung and brain were removed for macroscopic and microscopic analysis. The data were presented as mean ± standard error of mean. The comparison betweenthe values of blood counts and biochemical tests was performed by ANOVA followed by Tukey test, after verification of normality by the Kolmogorov Smirnov. The comparison between the pre and post operative of each group was performed by Student t test. Tocompare the microscopic changes, we used the Fisher exact test. All results were considered significant for a probability of significance greater than 95% (p < 0.05). As results it was found a decreasing on lymphocytes in groups 2, 3 and 4 and total leukocytes in groups 2 and 3, increasing of ALT in groups 2 and 3, of FA in Group 3 and GGT in Group 4. It was a decreasing of albumin in Group 4 and elevation of BBI in groups 3 and 4. An increasing of urea, lactate and CK were observed in groups 2, 3 and 4, and reduction of calcium in Group 4. Significant areas of hepatic degeneration were observed in all animals in Group 2 andfour animals in Group 3. All animals in Group 4 showed signs of hepatocellular necrosis. All rabbits in Group 2 showed areas of degeneration of renal tubules and all of the groups 2 and 3 showed dilation of blood vessels in the corticomedullary region of the kidney. Splenic congestion occurred in two animals in groups 2 and 3, and four animals in Group 4. Brain edema occurred in two animals in Group 3 and four animals in Group 4. In the lung, alveolar hyperinflation was observed in 4 animals in groups 2 and 3 and in all animals in Group 4. 100% of the animals with gastric ischaemia showed extensive areas of necrosis of the mucosa of the gastric body and bottom. In groups 3 and 4, there was necrosis of the muscle layer of three and four animals, respectively. Gastric necrosis was observed in three animals in Group 3 and Group 4. In conclusion, desvascularization of the stomach during more than 3 hours provokes necrosis and impaired gastric function and morphology, and causes serious injury to the liver, brain edema, pancreatic dysfunction, platelets reduction, lymphopenia, renal vasodilation and peritonitis.